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Resveratrol ameliorates iron overload induced liver fibrosis in mice by regulating iron homeostasis
This study is intended to explore the protective effects of resveratrol (RES) on iron overload-induced liver fibrosis and its mechanism. Iron dextran (50 mg/kg) was injected intraperitoneally in all groups except the control group. Mice in the L-RES, M-RES and H-RES groups were gavaged with RES solu...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
PeerJ Inc.
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9188311/ https://www.ncbi.nlm.nih.gov/pubmed/35698613 http://dx.doi.org/10.7717/peerj.13592 |
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author | Wang, Hua Jiang, Chuan Yang, Yakun Li, Jinghan Wang, Yihan Wang, Chaonan Gao, Yonggang |
author_facet | Wang, Hua Jiang, Chuan Yang, Yakun Li, Jinghan Wang, Yihan Wang, Chaonan Gao, Yonggang |
author_sort | Wang, Hua |
collection | PubMed |
description | This study is intended to explore the protective effects of resveratrol (RES) on iron overload-induced liver fibrosis and its mechanism. Iron dextran (50 mg/kg) was injected intraperitoneally in all groups except the control group. Mice in the L-RES, M-RES and H-RES groups were gavaged with RES solution at 25, 50 mg/kg and 100 mg/kg, respectively, 4 h before injection of iron dextran every day; mice in the deferoxamine (DFO) group were injected with DFO intraperitoneally (100 mg/kg); mice in the control group received isovolumetric saline. After seven weeks of RES administration, serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) activities and liver hydroxyproline (Hyp) levels were reduced; the malondialdehyde (MDA) activities decreased and the levels of superoxide dismutase (SOD) and glutathione (GSH) were raised. Hematoxylin and eosin (H&E), Prussian, and Masson staining indicated that RES treatment could improve cell damage and reduce hepatic iron deposition and collagen deposition in iron-overload mice. The expression of Bcl-2 was increased, the expression levels of Bax and caspase-3 were decreased under RES treatment. Moreover, RES reduced the expression of hepcidin, ferritin (Ft), divalent metal transporter-1 (DMT-1), transferrin receptor-2 (TFR-2), and raised the expression of ferroprotein-1 (FPN-1). In conclusion, RES could ameliorate iron overload-induced liver fibrosis, and the potential mechanisms may be related to antioxidant, anti-inflammatory, anti-apoptotic, and more importantly, regulation of iron homeostasis by reducing iron uptake and increasing iron export. |
format | Online Article Text |
id | pubmed-9188311 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | PeerJ Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-91883112022-06-12 Resveratrol ameliorates iron overload induced liver fibrosis in mice by regulating iron homeostasis Wang, Hua Jiang, Chuan Yang, Yakun Li, Jinghan Wang, Yihan Wang, Chaonan Gao, Yonggang PeerJ Toxicology This study is intended to explore the protective effects of resveratrol (RES) on iron overload-induced liver fibrosis and its mechanism. Iron dextran (50 mg/kg) was injected intraperitoneally in all groups except the control group. Mice in the L-RES, M-RES and H-RES groups were gavaged with RES solution at 25, 50 mg/kg and 100 mg/kg, respectively, 4 h before injection of iron dextran every day; mice in the deferoxamine (DFO) group were injected with DFO intraperitoneally (100 mg/kg); mice in the control group received isovolumetric saline. After seven weeks of RES administration, serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) activities and liver hydroxyproline (Hyp) levels were reduced; the malondialdehyde (MDA) activities decreased and the levels of superoxide dismutase (SOD) and glutathione (GSH) were raised. Hematoxylin and eosin (H&E), Prussian, and Masson staining indicated that RES treatment could improve cell damage and reduce hepatic iron deposition and collagen deposition in iron-overload mice. The expression of Bcl-2 was increased, the expression levels of Bax and caspase-3 were decreased under RES treatment. Moreover, RES reduced the expression of hepcidin, ferritin (Ft), divalent metal transporter-1 (DMT-1), transferrin receptor-2 (TFR-2), and raised the expression of ferroprotein-1 (FPN-1). In conclusion, RES could ameliorate iron overload-induced liver fibrosis, and the potential mechanisms may be related to antioxidant, anti-inflammatory, anti-apoptotic, and more importantly, regulation of iron homeostasis by reducing iron uptake and increasing iron export. PeerJ Inc. 2022-06-08 /pmc/articles/PMC9188311/ /pubmed/35698613 http://dx.doi.org/10.7717/peerj.13592 Text en ©2022 Wang et al. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, reproduction and adaptation in any medium and for any purpose provided that it is properly attributed. For attribution, the original author(s), title, publication source (PeerJ) and either DOI or URL of the article must be cited. |
spellingShingle | Toxicology Wang, Hua Jiang, Chuan Yang, Yakun Li, Jinghan Wang, Yihan Wang, Chaonan Gao, Yonggang Resveratrol ameliorates iron overload induced liver fibrosis in mice by regulating iron homeostasis |
title | Resveratrol ameliorates iron overload induced liver fibrosis in mice by regulating iron homeostasis |
title_full | Resveratrol ameliorates iron overload induced liver fibrosis in mice by regulating iron homeostasis |
title_fullStr | Resveratrol ameliorates iron overload induced liver fibrosis in mice by regulating iron homeostasis |
title_full_unstemmed | Resveratrol ameliorates iron overload induced liver fibrosis in mice by regulating iron homeostasis |
title_short | Resveratrol ameliorates iron overload induced liver fibrosis in mice by regulating iron homeostasis |
title_sort | resveratrol ameliorates iron overload induced liver fibrosis in mice by regulating iron homeostasis |
topic | Toxicology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9188311/ https://www.ncbi.nlm.nih.gov/pubmed/35698613 http://dx.doi.org/10.7717/peerj.13592 |
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